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    BIOMARKER:

    FLT3-ITD mutation

    i
    Other names: FLT3, Fms Related Tyrosine Kinase 3, Receptor-Type Tyrosine-Protein Kinase FLT3, Stem Cell Tyrosine Kinase 1, Fms-Like Tyrosine Kinase 3, CD135, FLK-2, STK1, Growth Factor Receptor Tyrosine Kinase Type III, Fetal Liver Kinase 2
    Entrez ID:
    2322
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    Related tests:
    6d
    Mutational landscape changes of AML in patients relapsing after allogeneic hematopoietic cell transplantation. (PubMed, Bone Marrow Transplant)
    Our findings indicate that while relapse after allo-HCT in AML is genetically diverse, timing of recurrence remains the most critical determinant of outcome. Given that certain genetic changes may inform therapeutic options, these findings highlight the relevance of longitudinal molecular monitoring especially during the early post-transplant period.
    Clinical • Journal
    |
    KRAS (KRAS proto-oncogene GTPase) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • DNMT3A (DNA methyltransferase 1)
    |
    KRAS mutation • FLT3-ITD mutation
    8d
    Efficacy and Safety of Lisafotoclax Plus Decitabine and Homoharringtonine in Venetoclax/Azacitidine Pretreated AML Patients (clinicaltrials.gov)
    P2, N=35, Not yet recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University
    New P2 trial
    |
    FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1)
    |
    FLT3-ITD mutation • NPM1 mutation
    |
    Venclexta (venetoclax) • azacitidine • decitabine • Synribo (omacetaxine mepesuccinate)
    9d
    Distinctive Molecular Risk Factors Between MDS and MDS/AML Defined by ICC. (PubMed, Am J Hematol)
    Since the IPSS-R and IPSS-M showed a poorly prognostic separation for MDS/AML patients, we further established a new prognostic model MDS/AML-IPSS-M and significantly improved its prognostic discrimination ability. Taking together, our research findings enhance the understanding of the molecular biology of MDS and can provide important guidance for the clinical identification of MDS/AML patients that might benefit clinical decision-making and therapeutic research.
    Journal
    |
    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3)
    |
    FLT3-ITD mutation
    11d
    TMLI-MA: Preparation for bone marrow transplant through the combined use of chemo and radiotherapy (intensive or myeloablative: eliminates stem cells) (2024-514484-25-00)
    P1/2, N=49, Recruiting, Fundacion Publica Andaluza Para La Gestion De La Investigacion En Salud De Sevilla | Not yet recruiting --> Recruiting
    Enrollment open
    |
    FLT3 (Fms-related tyrosine kinase 3) • HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1)
    |
    FLT3-ITD mutation
    |
    cyclophosphamide • etoposide IV • sirolimus
    13d
    Measurable residual disease testing in acute myeloid leukemia: current state, foundational models, and tools for future development. (PubMed, Cancer Metastasis Rev)
    While subtypes of AML are increasingly defined by druggable driver mutations including FLT3-ITD, IDH1, IDH2, and NPM1, conventional chemotherapy and reduced intensity induction regimens (e.g., azacitidine-venetoclax) remain therapeutic backbones. Current understanding of AML biology and state-of-the-art tools for MRD measurement are reviewed here in an effort to promote clinical and laboratory investigator collaboration for the development of reliable tools for improving outcomes in this deadly disease. Clinical trial number: not applicable.
    Review • Journal
    |
    FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1)
    |
    FLT3-ITD mutation
    |
    Venclexta (venetoclax) • azacitidine
    14d
    Novel staurosporine-type indolocarbazole glycoalkaloids as potent and selective FLT3-ITD inhibitors for acute myeloid leukemia. (PubMed, Eur J Med Chem)
    Among them, compound 35 showed the most potent inhibition against FLT3-ITD (IC₅₀ = 3.16 ± 0.49 nM) and FLT3-WT (IC₅₀ = 294.7 ± 14.5 nM), comparable to the clinical reference midostaurin, with a ∼93-fold selectivity index...Mechanistic studies demonstrated that compound 35 effectively suppressed FLT3 phosphorylation and downstream STAT5, Akt, and Erk signaling, induced G2/M cell-cycle arrest, and triggered apoptosis in FLT3-ITD-positive AML cells. Taken together, these findings identify compound 35 as a potent and selective FLT3 inhibitor and establish a promising scaffold for the development of next-generation therapeutics against FLT3-driven leukemias.
    Journal
    |
    FLT3 (Fms-related tyrosine kinase 3)
    |
    FLT3-ITD mutation
    |
    midostaurin
    14d
    Genetic alterations and measurable residual disease in core binding factor acute myeloid leukemia. (PubMed, Leukemia)
    These results were confirmed in the CBF-2006 validation cohort. KIT-TKD mutations in RUNX1::RUNX1T1 and FLT3-ITD in CBFB::MYH11 worsen prognosis independently of MRD and must be included in risk stratification of CBF AMLs.
    Clinical • Journal
    |
    FLT3 (Fms-related tyrosine kinase 3) • RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
    |
    FLT3-ITD mutation • FLT3 mutation • RUNX1 mutation
    14d
    Extramedullary manifestations of acute promyelocytic leukaemia at initial diagnosis: an autopsy analysis. (PubMed, BMJ Case Rep)
    Despite prompt initiation of all-trans retinoic acid and arsenic trioxide therapy, she developed worsening respiratory distress and neurological deterioration, succumbing within 70 hours of admission...The optimal management strategies remain undefined, particularly for CNS-directed therapy. This case underscores the importance of considering extramedullary involvement in APL patients with atypical or rapidly progressive presentations.
    Journal
    |
    FLT3 (Fms-related tyrosine kinase 3)
    |
    FLT3-ITD mutation
    |
    arsenic trioxide
    15d
    Revumenib in Combination With 7+3 + Midostaurin in AML (clinicaltrials.gov)
    P1, N=22, Recruiting, Richard Stone, MD | Trial completion date: Mar 2027 --> Mar 2028 | Trial primary completion date: Mar 2026 --> Mar 2027
    Trial completion date • Trial primary completion date
    |
    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • SRSF2 (Serine and arginine rich splicing factor 2) • CREBBP (CREB binding protein) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • KAT6A (Lysine Acetyltransferase 6A) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
    |
    TP53 mutation • FLT3-ITD mutation • NPM1 mutation • Chr del(5q)
    |
    midostaurin • daunorubicin • Revuforj (revumenib)
    15d
    VAG-3+7-G: VAG Versus Standard Chemotherapy With FLT3 Inhibitor in Adult Patients With FLT3-Mutated AML (clinicaltrials.gov)
    P3, N=300, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China | Initiation date: Jan 2026 --> Apr 2026
    Trial initiation date
    |
    FLT3 (Fms-related tyrosine kinase 3) • BCL2 (B-cell CLL/lymphoma 2)
    |
    FLT3-ITD mutation • FLT3-TKD mutation
    |
    Venclexta (venetoclax) • cytarabine • Xospata (gilteritinib) • azacitidine • daunorubicin • idarubicin hydrochloride
    16d
    FLT3-ITD scaffolds PKCι-STAT1 to drive noncanonical S727 phosphorylation and CD276-driven CD8+ T-cell exhaustion in AML. (PubMed, Blood)
    In patient-derived xenograft models, co-treatment with FLT3i (quizartinib) and CD276-targeting agents led to 72.9%-80.4% tumor burden reduction and enhanced CD8+ T cell function, outperforming quizartinib monotherapy. These findings define a scaffolded PKCι-pS727-STAT1 signaling axis that promotes immune evasion in FLT3-ITD AML, supporting combined FLT3 and CD276 targeting as a promising translational strategy in this aggressive leukemia subtype.
    Journal
    |
    FLT3 (Fms-related tyrosine kinase 3) • CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD276 (CD276 Molecule) • STAT1 (Signal Transducer And Activator Of Transcription 1)
    |
    FLT3-ITD mutation
    |
    Vanflyta (quizartinib)
    16d
    Autophagy inhibition potentiates the antileukemic effect of FLT3 inhibitors and overcomes resistance in FLT3-ITD acute myeloid leukemia. (PubMed, Cell Death Discov)
    In FLT3-ITD AML cell lines (MOLM13 and MV4-11), treatment with first- and second-generation FLT3i (midostaurin and quizartinib, respectively) induced autophagy. The combination of quizartinib and chloroquine demonstrated a synergistic effect in MV4-11QR cells and this effect was associated with greater inhibition of the FLT3 receptor compared to the monotherapies. Therefore, combining FLT3i with autophagy inhibition enhances the FLT3i antileukemic efficacy and overcomes pharmacological resistance.
    Journal
    |
    FLT3 (Fms-related tyrosine kinase 3) • ATG5 (Autophagy Related 5) • ATG7 (Autophagy Related 7) • RFC4 (Replication Factor C Subunit 4)
    |
    FLT3-ITD mutation
    |
    midostaurin • Vanflyta (quizartinib) • chloroquine phosphate